Meditation Performance and Critical Care: Scott Weingart

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The document discusses the results of a study on the impact of COVID-19 lockdowns on air pollution. Researchers found that lockdowns led to significant short-term reductions in nitrogen dioxide and fine particulate matter pollution globally as economic activities slowed. However, the impacts on greenhouse gases and long-term air quality improvements remain uncertain without permanent behavior and economic changes.

Santé & Médecine

Meditation Performance and Critical Care: Scott Weingart

Meditation Performance and Critical Care: Scott Weingart

Meditation Performance and Critical Care: Scott Weingart

Meditation Performance and Critical Care: Scott Weingart

Meditation Performance and Critical Care: Scott Weingart

Meditation Performance and Critical Care: Scott Weingart

Meditation Performance and Critical Care: Scott Weingart

Meditation Performance and Critical Care: Scott Weingart

Meditation Performance and Critical Care: Scott Weingart

Meditation Performance and Critical Care: Scott Weingart

Meditation Performance and Critical Care: Scott Weingart

Meditation Performance and Critical Care: Scott Weingart

Meditation Performance and Critical Care: Scott Weingart

Meditation Performance and Critical Care: Scott Weingart

Meditation Performance and Critical Care: Scott Weingart

Meditation Performance and Critical Care: Scott Weingart

Meditation Performance and Critical Care: Scott Weingart

Meditation Performance and Critical Care: Scott Weingart

Meditation Performance and Critical Care: Scott Weingart

Meditation Performance and Critical Care: Scott Weingart

Meditation Performance and Critical Care: Scott Weingart

Meditation Performance and Critical Care: Scott Weingart

Meditation Performance and Critical Care: Scott Weingart

Meditation Performance and Critical Care: Scott Weingart

Meditation Performance and Critical Care: Scott Weingart

Meditation Performance and Critical Care: Scott Weingart

Meditation Performance and Critical Care: Scott Weingart

Meditation Performance and Critical Care: Scott Weingart

Meditation Performance and Critical Care: Scott Weingart

Meditation Performance and Critical Care: Scott Weingart

Meditation Performance and Critical Care: Scott Weingart

Meditation Performance and Critical Care: Scott Weingart

Meditation Performance and Critical Care: Scott Weingart

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En vedette

Katrin Hruska discusses the usefulness of biomarkers in Emergency Medicine. All biomarkers are awesome predictors of badness. Elevated hS-troponins after non-cardiac surgery or an acute exacerbation of COPD are associated with increased mortality. In seemingly healthy people, elevated D-dimer levels are associated with increased mortality. Similarly, NT-proBNP levels predict mortality in patients with end-stage renal disease. A biomarker, in its broadest sense, is defined as “a characteristic that is objectively measured and evaluated as an indicator of normal biological processes, pathogenic processes, or pharmacologic responses to a therapeutic intervention” (NIH Biomarkers Definitions Working group, 2001). This definition includes everything from laboratory tests to blood pressure measurements or an ultrasound scan. The clinical assessment in the Emergency Department is based on the subjective history of the patient and all available biomarkers (and their change over time). If we assume that biomarkers are objectively measured, there is an overestimation of their individual importance. As Katrin explains, over testing and over diagnosis have serious consequences. Not only for patients but also for the healthcare system. In a clinical context the ease of getting a laboratory test leads to a lower threshold for testing. This increases testing without affecting relevant clinical endpoints. Also, when a biomarker becomes part of the standardised workup for a certain symptom, primary care centres and emergency telephone services will refer patients to the Emergency Department for testing, even when the pretest probability is low. Katrin contends this bias is not an inherent problem of biomarkers themselves, but of the decision-making process of clinicians. The human brain fears uncertainty. Anything that adds to the feeling of knowing is rewarding, which is the most probable explanation of over testing in settings where medico-legal risks for the clinicians are low. There is an ever-increasing number of patients seeking to rule out serious conditions by relying on biomarker testing to provide certainty.

Biomarkers in Emergency Medicine: Katrin Hruska

Biomarkers in Emergency Medicine: Katrin Hruska

Biomarkers in Emergency Medicine: Katrin Hruska

SMACC Conference

Anand Swaminathan and Iain Beardsell debate the use of thrombolytics in the treatment of submassive pulmonary embolism (PE). PE is a spectrum of disease. Patients should be treated differently depending on where they are on the spectrum. Subsegmental PE may need no treatment at all, whereas massive PE is unlikely to improve without thrombolytics. Anand argues for the use of thrombolytics. Evidently, time is critical when dealing with patients and Anand posits that thrombolytics gives the physician control over time. Submassive PE can deteriorate, leading to massive pulmonary embolism. A proportion of these patients will die. The data is not conclusive for the use of thrombolytics in terms of mortality, however long term outcomes do improve. Finally, Anand concludes by suggesting that the decision to use thrombolytics relies on sound clinical reasoning and decision making, informed by the available data. He argues for nuanced treatments and use of these drugs. Iain takes a different approach in his reply. Some of the most difficult topics in medicine attract considerable debate. The use of thrombolysis for submassive PE is one of these. In this argument Iain attempts to highlight some of the most pertinent evidence against the use of thrombolysis. And he does so through song! Submassive PE should be Thrombolysed: Anand Swaminathan and Iain Beardsell For more like this, head to our podcast page. #CodaPodcast

Submassive PE should be Thrombolysed

Submassive PE should be Thrombolysed

Submassive PE should be Thrombolysed

SMACC Conference

Powerpoints and Meth

Powerpoints and Meth

Powerpoints and Meth

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Peter Brindley explains how burnout affects us all. It affects the cost, quality of care, organisational culture, performance and patient outcomes. Burnout is fatigue, loss of ideals, purposelessness, presentism and the sense of being under-appreciated. It is not tiredness, exhaustion, boredom, mid-life crisis, depression, PTSD, perfectionism or narcissism. Moreover, burnout involves the 4 C's: cutting corners, cynicism, callousness, and contempt. Peter explains when and why, and to whom a burnout occurs. A major reason for burnout is the difference between expectations and reality. This drives the thought, “this is not what I signed up for.” Furthermore, he presents the 12 steps which lead to a burnout. It begins by the need to prove yourself by working harder, neglecting your needs, avoiding issues, and losing friends or hobbies. This leads to denial, withdrawal, behavioural changes, depersonalisation, inner emptiness, depression and finally burnout. Peter suggests a few things that we can do to prevent burnout. He recommends purposeful imbalance and dividing career into thirds: learning, earning, and returning. Evidently, burnout is a chronic condition, and although it cannot be cured, it is manageable. It might take years to manifest and hence, we must always be on the lookout for the signs. Finally, for more like this head to our podcast page. #CodaPodcast

Burnout in Healthcare: Peter Brindley

Burnout in Healthcare: Peter Brindley

Burnout in Healthcare: Peter Brindley

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Trish Woods guides you through some clinical pearls in the intensive care management of neonates. The complex physiology of the transitioning required in the journey from foetal life to neonatal presents many challenges and scary moments. Trish helps you to navigate these challenges and to unlock the key to providing quality neonatal intensive care. Many things can go wrong in the neonatal period as babies transition to life in the real world. Trish highlights her thoughts on the use of positive end expiratory pressure (PEEP), how deep to intubate, when to clamp the cord and the use of ultrasound. When babies arrive early their lungs can be full of meconium or fluid. Due to this, Trish recommends using PEEP – without which there is distal airway collapse and fluid accumulation. Aeration of the lungs is vital. To this end, how deep should intubation be aimed? The depth may not be overly important. This is because regional lung aeration triggers widespread, global increase in pulmonary blood flow. There is little definitive evidence to guide clinicians on when to clamp the cord – early or late. Trish recommends considering the physiology of clamping the cord. After clamping the cord there is a massive drop in cardiac output. Ventilatory support will turn this around – something to remember. In a compromised baby, perhaps we should aim to clamp the cord sooner and then initiate ventilation. Finally, Trish highlights the utility of ultrasound. Viewing the heart and lungs provides crucial information for the clinician. Furthermore, Trish discusses actively looking for aeration, collapse, consolidation and pneumothorax in the lungs and thorax. Overall, don’t forget the essentials. Trish reminds you to keep life sweet, warm, and tempting and help neonates to transition into the big world. Neonatal Intensive Care: Trish Woods For more like this, head to our podcast page. #CodaPodcast

Neonatal Intensive Care: Trish Woods

Neonatal Intensive Care: Trish Woods

Neonatal Intensive Care: Trish Woods

SMACC Conference

First Amoung Equals: A Tribute to Dr John Hinds

First Amoung Equals: A Tribute to Dr John Hinds

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SMACC Conference

The use of adrenaline in cardiac arrest resuscitation has been advocated since the 1960s. Laboratory studies and anecdotal experience showed improved rates of return of spontaneous circulation (ROSC) with the use of adrenaline at a dosage of approximately 0.01 mg/kg. This led to the widespread adoption of adrenaline administration during cardiac arrest into every resuscitation guideline for decades to come. Extensive laboratory studies characterized the beneficial physiological effects of adrenaline during cardiac arrest and closed-chest cardiopulmonary resuscitation (CC-CPR). Adrenaline administered during CC-CPR results in peripheral arterial vasoconstriction that raises the aortic pressure, particularly during the relaxation phase of CC-CPR. This increase in aortic pressure results in an increased aortic to right atrial pressure gradient that drives blood flow to the myocardium during CC-CPR. This pressure gradient is known as the coronary perfusion pressure (CPP) and has been shown to correlate with ROSC in both laboratory investigations and clinical studies. During the 1990s, the use of “high-dose” adrenaline showed increased rates of ROSC compared to “standard-dose” adrenaline. However, it was subsequently recognized that larger doses of adrenaline did not result in improved survival. Furthermore, questions have been raised as to whether or not “standard-dose” adrenaline improves survival from cardiac arrest. Recent meta-analyses have raised serious questions about the value of adrenaline, showing a benefit for achieving ROSC but no clear evidence of improved long-term survival. Controlled clinical trials to address this question are now underway. However, there is another important issue that needs to be addressed: the “route” of administration. With the growing interest in endovascular resuscitation, the use of intra-aortic adrenaline titration offers a means of rapidly and effectively delivering adrenaline to peripheral arterial effector sites while providing arterial pressure and CPP monitoring to guide titration of adrenaline doses to achieve an optimal hemodynamic effects while avoiding excessive adrenaline doses. To enable screen reader support, press shortcut Ctrl+Alt+Z. To learn about keyboard shortcuts, press shortcut Ctrl+slash.

Rethinking Adrenaline in Cardiac Arrest

Rethinking Adrenaline in Cardiac Arrest

Rethinking Adrenaline in Cardiac Arrest

SMACC Conference

Andrew Naidech - Intracerebral Hemorrhage: Down, Not Out

Andrew Naidech - Intracerebral Hemorrhage: Down, Not Out

Andrew Naidech - Intracerebral Hemorrhage: Down, Not Out

SMACC Conference

Awake Intubation the EMCrit Way

Awake Intubation the EMCrit Way

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Error is almost inevitable in our clinical practice so we should be prepared to help and prepare those individuals involved for the benefit of them, our systems and our patients. Do you remember that patient you saw last night?': A phrase the strikes terror into the hearts of all physicians. The prospect of a patient coming to harm as a result of a mistake is terrifying but it can and does happen. The consequences for the patient and their family are often tragic but what of the clinicians who made the error? For many the result of making a terrible error is life changing. Those permanently harmed by error are often referred to as second victims with the consequences of terrible events being life-long. This talk explores the predictable course for clinicians who are involved in error and asks whether we can prepare and support such individuals through a difficult time.

Coping with a Terrible Error by Simon Carley

Coping with a Terrible Error by Simon Carley

Coping with a Terrible Error by Simon Carley

SMACC Conference

Don't Forget A & B! Over 500,000 patients per year suffer sudden cardiac arrest. Despite advances in our understanding and management of cardiac arrest, less than 15% of patients survive to hospital discharge with meaningful neurologic survival. In recent years, the focus of cardiac arrest resuscitation has been the delivery of high-quality chest compressions and early defibrillation for those with a shockable rhythm. As a result, airway interventions and ventilation now follow attempts to optimize circulation in cardiac arrest patients. Though high-quality CPR and early defibrillation are essential in the initial stages of resuscitation, advanced airway placement and appropriate ventilation are critical to overall patient survival. Dr. Winters' discusses the current literature on the timing of advanced airway placement, oxygenation, and ventilation for the cardiac arrest patient. In addition, he discusses optimal targets for oxygenation and ventilation in the patient with return of spontaneous circulation from sudden cardiac arrest.

Mike Winters - Don’t Forget A and B!

Mike Winters - Don’t Forget A and B!

Mike Winters - Don’t Forget A and B!

SMACC Conference

What is the problem? Delivering bad news and having an end of life conversation are core skills for any practitioner who deals with critically ill patients. Current data show that while 22% of deaths in the USA now occur in ICU, 54% of families surveyed have a poor understanding of patient’s diagnosis, treatment plan and prognosis. Dr. Kate Granger found this out first hand while admitted to hospital in the UK and started the #hellomynameis campaign. What is the evidence? While families feel more validated if given longer to speak, doctors speak for 71% of the time in family meetings. -Longer meetings are also associated with greater patient and family member satisfaction. -Patients perceive that doctors spend longer with them if the doctor is sitting down. -Use of a simple mnemonic increases satisfaction and reduced the incidence of PTSD in family members. What do experts do? 1. Prepare for the meeting. Decide who will attend, what you will talk about and what your goals are. 2. Introduce everyone and explain the agenda. 3. Gather everyone’s understanding 4. Listen and don’t interrupt5Empathise (physicians express no empathy in 1/3 of family meetings) 6. Make the patient’s voice heard 7. Make your recommendation to go forward 8. Reflect on the meeting after it concludes What about the difficult situations? Hope is an issue that comes up often. Many other specialties emphasise the importance of hope, while intensivists are often seen as being nihilistic. But we can still foster a degree of hope in patients and families without being unrealistic. -Techniques for managing conflict are discussed such as identifying discord in the family and avoiding mixed messages from staff. -The importance of spirituality is discussed.

Breaking Bad (News) by David Anderson

Breaking Bad (News) by David Anderson

Breaking Bad (News) by David Anderson

SMACC Conference

Goodbye GCS! Summary by: Mark Wilson Consciousness comprises “wakefulness” (that’s the brain stem, opening your eyes component) and “content” (that’s the supratentorial, thinking, “someone’s home” component). You can have wakefulness without content (e.g. persistent vegetative state) but not content without wakefulness. Describing a “level” of consciousness, converting this multifaceted human brain ability into a linear scale was possibly the biggest neuroscience break through of the 20th Century. The 1974 Lancet paper in which Brian Jennet and Sir Graham Teasdale proposed the Glasgow Coma Scale (GCS) is certainly the most cited neuroscience paper. We had even put a man on the moon before this had been created. It’s relative simplicity and repeatability meant GCS was rapidly taken up across the world. Now 40 years on, is it out of date? There are problems with the GCS – it doesn’t include pupil response, it doesn’t look at ventilation or other autonomic functions hence other systems such as the 4 score system have been proposed. But these take longer, and are poorly known so cannot be used like GCS to rapidly convey in a meaningful way the level of consciousness of a patient between clinicians. In this talk Mark Wilson goes through the history of the GCS and other conscious measures… is it time to say Goodbye to GCS?

Goodbye GCS! - Mark Wilson

Goodbye GCS! - Mark Wilson

Goodbye GCS! - Mark Wilson

SMACC Conference

Martin Smith The management of severe traumatic brain injury (TBI) has undergone extensive revision following evidence that longstanding and established practices are not as efficacious or innocuous as previously believed. Very few specific interventions have been shown to improve outcome in large randomized controlled trials and, with the possible exception of avoidance of hypotension and hypoxaemia, most are based on observational studies or analysis of physiology and pathophysiology. Further, the substantial temporal and regional pathophysiological heterogeneity after TBI means that some interventions may be ineffective, unnecessary or even harmful in certain patients at certain times. Improved understanding of pathophysiology and advances in neuromonitoring and imaging techniques have led to the introduction of more effective and individualised treatment strategies that have translated into improved outcomes for patients. In particular, the sole goal of identifying and treating intracranial hypertension has been superseded by a focus on the prevention of secondary brain insults using a systematic, stepwise approach to maintenance of adequate cerebral perfusion and oxygenation. As well as being used to guide treatment interventions, multimodal neuromonitoring also gives clinicians confidence to withhold potentially dangerous therapy in those with no evidence of brain ischemia/hypoxia or metabolic disturbance. The days of blind adherence to generic physiological targets in the management of severe TBI have been replaced by an individualised approach to optimisation of physiology which has translated into improved outcomes for patients. Mark Wilson The New England Journal of Medicine has published a number of articles recently that demonstrate no benefit from classic neurotrauma interventions (ICP monitoring, cooling, decompression). This is because factors such as ICP and CPP are associated with bad outcome by association rather than causation. This debate will demonstrate that critical care just complicates things and it is high time for the randomised trial between the very best Neurocritical care and NOB therapy (Naso-pharyngeal, Oxygen and a Blanket).

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Adrian Plunkett describes how to learn from excellence in critical care. Learning from excellence is an initiative which began at Birmingham Children’s Hospital. Firstly, Adrian shares an anecdote regarding how the initiative begun. He sent a letter to the CEO of a hospital appreciating one of the doctors who treated him for cancer. The doctor unfortunately never received it. This caused Adrian to ask - is appreciation and gratitude undervalued? Evidently, noticing excellence will lead to two things: learning new insights and increasing staff morale. Adrian raises the question, why we do we not focus on the good things? We spend all our time improving safety and quality even though accidents and disasters are only a small percentage of what we do. Moreover, Adrian claims that people inherently have negative biases. This is evident in healthcare, so how can we combat this? The solution is to focus on excellent care. This led to the formation of a reporting system called Learning from Excellence (LfE), where people answer two questions: Who did something excellent? What did they do? LfE is a formal system for reporting and providing positive feedback and appreciation to the healthcare workers. It is a beneficial and constructive way of learning from excellence. Finally, Adrian explains, “Saying ‘thank you’ or ‘well done’ is the easiest quality improvement intervention of all.” Learning from excellence in critical care by Adrian Plunkett For more like this head to our podcast page. #CodaPodcast

Learning from excellence in critical care

Learning from excellence in critical care

Learning from excellence in critical care

SMACC Conference

The application of ‘CPR-for-all’ is the ultimate evidence drift. A treatment that is completely appropriate for dropping dead whilst running a marathon has almost no place in acute healthcare facilities where chronic irreversible complex co-morbidities abound. 90% of doctors would not choose CPR for themselves, yet 100% are trained in how to administer it to patients. Defaulting to ‘CPR-for-all’ removes a patients’ ability to provide informed consent for assault whilst they die from another disease. Remember - 2 weeks in ICU can spare you 5 minutes of difficult conversation. vs. Across the globe, patients are assumed to be full code to allow for prompt resuscitation, until code status can be discussed and clarified. There are numerous excellent reasons for this. Can you imagine if our systems decreed that DNR was the default? “Let’s not shock that VF, until we can clarify his code status.” Or, “let’s not resuscitate that child, after all, DNR is the default and her mother isn’t here yet!” Making DNR the default is not a good solution to ICU or hospital over-crowding. Let’s not mandate DNR, let’s mandate having reasonable code discussions early and often.

DNR Should Be The Default - PRO: Alex Psirides, CON: Sara Gray

DNR Should Be The Default - PRO: Alex Psirides, CON: Sara Gray

DNR Should Be The Default - PRO: Alex Psirides, CON: Sara Gray

SMACC Conference

En vedette (16)

Biomarkers in Emergency Medicine: Katrin Hruska

Biomarkers in Emergency Medicine: Katrin Hruska

Biomarkers in Emergency Medicine: Katrin Hruska

Submassive PE should be Thrombolysed

Submassive PE should be Thrombolysed

Submassive PE should be Thrombolysed

Powerpoints and Meth

Powerpoints and Meth

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Burnout in Healthcare: Peter Brindley

Burnout in Healthcare: Peter Brindley

Burnout in Healthcare: Peter Brindley

Neonatal Intensive Care: Trish Woods

Neonatal Intensive Care: Trish Woods

Neonatal Intensive Care: Trish Woods

First Amoung Equals: A Tribute to Dr John Hinds

First Amoung Equals: A Tribute to Dr John Hinds

First Amoung Equals: A Tribute to Dr John Hinds

Rethinking Adrenaline in Cardiac Arrest

Rethinking Adrenaline in Cardiac Arrest

Rethinking Adrenaline in Cardiac Arrest

Andrew Naidech - Intracerebral Hemorrhage: Down, Not Out

Andrew Naidech - Intracerebral Hemorrhage: Down, Not Out

Andrew Naidech - Intracerebral Hemorrhage: Down, Not Out

Awake Intubation the EMCrit Way

Awake Intubation the EMCrit Way

Awake Intubation the EMCrit Way

Coping with a Terrible Error by Simon Carley

Coping with a Terrible Error by Simon Carley

Coping with a Terrible Error by Simon Carley

Mike Winters - Don’t Forget A and B!

Mike Winters - Don’t Forget A and B!

Mike Winters - Don’t Forget A and B!

Breaking Bad (News) by David Anderson

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Breaking Bad (News) by David Anderson

Goodbye GCS! - Mark Wilson

Goodbye GCS! - Mark Wilson

Goodbye GCS! - Mark Wilson

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Learning from excellence in critical care

Learning from excellence in critical care

Learning from excellence in critical care

DNR Should Be The Default - PRO: Alex Psirides, CON: Sara Gray

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Precision Medicine in Acute Brain Injury

Precision Medicine in Acute Brain Injury

Precision Medicine in Acute Brain Injury

SMACC Conference

CORTICAL SPREADING DEPOLARISATION IN NEUROLOGICAL DISEASE – AN INTRODUCTION By Toby Jeffcote Cortical spreading depolarization (CSD) is a spreading loss of ion homeostasis, altered vascular response, change in synaptic architecture, and subsequent depression in electrical activity following an inciting neurological injury. It was first described by Leão in 1944, a disturbance in neuronal electrophysiology has since been demonstrated in a number of animal studies, and recently a few human studies that examine the occurrence of this depolarizing phenomenon in the setting of a variety of pathological states, including migraines, cerebrovascular accidents, epilepsy, intracranial hemorrhages, and traumatic brain injuries. The onset of CSD has been demonstrated experimentally following a disruption in the neuronal environment leading to glutamate-induced toxicity. This initial event leads to pathological changes in the activity of ion channels that maintain membrane potential. Recovery mechanisms such as sodium-potassium pumps that aim to restore homeostasis fail, leading to osmolar shifts of fluid, swelling of the neuron, and ultimately a measurable depression in cortical activity that spreads in the order of millimeters per minute. Equally important is the resulting change in vascular response. In healthy tissue, increased electrical activity is coupled with release of vasodilatory factors such as nitric oxide and arachidonic acid metabolites that increase local blood flow to meet increased energy expenditure. In damaged tissue, not only is the restorative vascular response lacking but a vasoconstrictive response is promoted and the ischemia that follows adds to the severity of the initial injury. Tissue threatened by this ischemic response is then at elevated risk for CSD propagation and falls into a vicious cycle of electrical and hemodynamic disturbance. Efforts have been made to halt this spreading cortical depression using N-methyl-D-aspartate receptor antagonists and other ion channel blockers to minimize the damaging effects of CSD that can persist long after the triggering insult.

CSD by Jeffcote Coda 22.pdf

CSD by Jeffcote Coda 22.pdf

CSD by Jeffcote Coda 22.pdf

SMACC Conference

Subdural Haemorrhage and MMA embolisation

Subdural Haemorrhage and MMA embolisation

Subdural Haemorrhage and MMA embolisation

SMACC Conference

Andy Neill - More neuroanatomy pearls for neurocritical care

Andy Neill - More neuroanatomy pearls for neurocritical care

Andy Neill - More neuroanatomy pearls for neurocritical care

SMACC Conference

Andrew Udy talks about Brain Tissue Oxygen Monitoring: It’s Not What You’ve Got It’s What You Do With It The BONANZA Trial Andrew Udy talks about the ongoing BONANZA Trial which is assessing whether an algorithm that incorporates both ICP and brain tissue oxygen (PbTO2) can improve outcomes after traumatic brain injury (TBI). Like with all monitoring, how the PbTO2 is interpreted and managed is critical and the devil is in the detail! More on BONANZA here More on BOOST3 here

The BONANZA Trial and PbTO2 Monitoring

The BONANZA Trial and PbTO2 Monitoring

The BONANZA Trial and PbTO2 Monitoring

SMACC Conference

R. Loch Macdonald, M.D., Ph.D. Community Neurosciences Institute Fresno, California, USA Angiographic vasospasm and more accurately, delayed cerebral ischemia, continue to contribute to morbidity and mortality in patients with aneurysmal subarachnoid hemorrhage (SAH). It is known that angiographic vasospasm is common after SAH, occurring in two-thirds of patients. Cerebral infarctions that developed days after the SAH have been attributed to angiographic vasospasm, occuring in about a third of patients, although this has always been controversial. Angiographic vasospasm theoretically can only damage the brain by restricting blood flow but there is no easy, accurate, widely available method to measure cerebral blood flow and this is not the measurement we need. Blood flow depends on metabolic demand so what we need to know to determine if angiographic vasospasm is causing ischemia is oxygen extraction fraction in the brain tissue supplied the the spastic artery. Without this measurement, the attribution of ischemia to vasospasm is subjective. Since angiographic vasospasm is essentially the only detectable delayed phenomenon after SAH, we focus on it and apply tremendous resources to preventing or reversing the vasospasm. Undoubtedly angiographic vasospasm can cause cerebral infarctions, but it has to be severe and flow limiting. But SAH is a complex disease. There are many other causes for cerebral infarctions after SAH, the most common being due to the aneurysm repair procedure. And a given degree of vasospasm may cause infarction in a volume-depleted patient with poor collateral blood supply but not in a patient without these things. There also are hypodense brain lesions after SAH that are due to intracerebral hemorrhages. There can be hypodensities in the brain directly under usually thick SAH where the brain dies. This observation in particular supports a role for cortical spreading depolarizations/ischemia as a cause of infarction after SAH. Other macromolecular processes that are hypothesized to cause brain damage after SAH include microthromboembolism, changes in the microcirculation, delayed brain cell apoptosis and capillary transit time heterogeneity. Determining the importance of these things is hindered by the lack of an easy way to detect them in patients. It is also known that poor grade patients, who presumably have more early brain injury and ischemia than good grade patients, are more prone to delayed cerebral ischemia, suggesting increased sensitivity to secondary insults of the already injured brain. We also assume delayed neurological deterioration when attributed to vasospasm or delayed cerebral ischemia, is purely due to ischemia. While knowledge about what happens pathophysiologically after SAH is increasing, management of delayed cerebral ischemia still focuses on detecting angiographic vasospasm and then augmenting the blood pressure to improve cerebral blood flow or dilating the spastic arteries with balloons or drugs.

Dilating the Dogma of Vasospasm

Dilating the Dogma of Vasospasm

Dilating the Dogma of Vasospasm

SMACC Conference

EVD Tips and Tricks

EVD Tips and Tricks

EVD Tips and Tricks

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Part 2 of a debate over the classification of TBI. Andrew Udy then argues that this classification is fundamentally flawed. He discusses the issues with the Glasgow Coma Scale, and therefore the follow-on issues in TBI classification, including all the confounders to the GCS, the issues with timing of the score as well as GCS not taking baseline function or specifics subtypes of TBI into account. He makes teh argument that biomarkers may better categorise the diffuse entity we call TBI.

There is no such thing as mild, moderate and severe TBI - by Andrew Udy

There is no such thing as mild, moderate and severe TBI - by Andrew Udy

There is no such thing as mild, moderate and severe TBI - by Andrew Udy

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Andrew Chow, Intensivist with a neurosurgical background, argues that the current categorisation system for traumatic brain injury (TBI) works, and makes sense! He tackles us through the history of this system, and why it’s important to differentiate different types of TBI. The arguments in favour of this categorisation include the consistency and benefits of a universal language, the implications for triage and management, and the fact that this system has been endorsed by all major organisations

TBI Debate - Mild, moderate and severe categories work

TBI Debate - Mild, moderate and severe categories work

TBI Debate - Mild, moderate and severe categories work

SMACC Conference

Dr Nick Little is an experienced Neurosurgeon who's looked after patients with traumatic brain injury for his whole career. Here he discusses the difficulties of prognostication following traumatic brain injury (TBI). He talks about the statistics of outcomes following mild, moderate and severe TBI and then goes on to tackle the harder topic of how we try to work out what an individual would want if they knew the spectrum of outcomes that they may face. The issues with the clinical examination findings we use to prognosticate are covered, as well as which imaging findings he finds most helpful. He also mentions the difficulties with current prognostic calculators.

TBI: when to stop and when to give time

TBI: when to stop and when to give time

TBI: when to stop and when to give time

SMACC Conference

Historically, when it came to brain injury, ketamine had a bad rap. Much of that dogma was dispelled in the last decade, and ketamine is now frequently used as an induction agent in acute brain injury, especially traumatic brain injury, due to it’s favorable effects on haemodynamics. However a new application of ketamine is now being explored - whether ketamine may be able to reduce secondary brain injury.

Ketamine in Brain Injury by Toby Jeffcote

Ketamine in Brain Injury by Toby Jeffcote

Ketamine in Brain Injury by Toby Jeffcote

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20 million people around the world are living with a spinal cord injury (SCI). The medical issues they develop over the years differ to any other patient cohort. These complications include autonomic dysreflexia, management of pressure areas, specific infections, nuanced peri-operative care and highly specific issues such as baclofen pump management and syringomyelia Do look at the NeuroResus section on this and listen to Spinal Rehab Specialist Bonne Lee talk about this side of SCI care. Keywords SCI, spinal, spinal cord injury, autonomic dysreflexia, pressure areas, infection, peri-operative care, baclofen pump, syringomyelia, chronic SCI, spinal trauma, spinal rehab, incomplete SCI

Managing Complications of Chronic SCI by Bonne Lee

Managing Complications of Chronic SCI by Bonne Lee

Managing Complications of Chronic SCI by Bonne Lee

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Tania is a neurologist and epileptologist with expertise in continuous EEG (cEEG) and status epilepticus (SE). This talk covers what a seizure is, what status is, including focal and generalised status epilepticus. So why do we do cEEGs for patients with suspected SE? To confirm the diagnosis To see if patient just post ictal or still seizing To establish that the clinical and electric seizures have stopped To see if burst suppression is achieved To exclude other differential diagnoses She makes a good argument for why cEEG is such an important tool in managing SE. In the questions after the talk, the issue of availability of cEEG in the Australian setting was discussed. Limited montage EEGs are discussed including their pros and cons.

EEG and Status Eplilepticus by Tania Farrar

EEG and Status Eplilepticus by Tania Farrar

EEG and Status Eplilepticus by Tania Farrar

SMACC Conference

Stuart Browne is a Neuro Rehab specialist from Sydney. These slides accompany a talk he gave at the Brian Symposium in 2023. He discusses what "severe disability" really means. Severe disability is more common than many realise - about 6% of the Australian population. Stuart discusses how health is more than simply physical recovery and how it is a multidimensional construct. He covers how permanent disability doesn't necessarily equate to a poor quality of life. He also discusses the long timespan of recovery, which is often much longer than appreciated. He specifically discusses "Locked-in Syndrome" and how the survivors have surprisingly positive self-reported health-related quality of life and well-being. Stuart also covers how severely disabled people face various forms of discrimination.

Browne Neuro symposium.pptx

Browne Neuro symposium.pptx

Browne Neuro symposium.pptx

SMACC Conference

Paediatric Stroke by Shree Basu

Paediatric Stroke by Shree Basu

Paediatric Stroke by Shree Basu

SMACC Conference

After spinal cord injury (SCI), there aren’t many interventions we have available that actually make a difference. Augmenting blood pressure to increase spinal cord perfusion pressure is an attractive concept that may improve neurological outcomes following SCI. We know that hypotension can make SCI worse. Clinical studies looking at blood pressure augmentation are mostly old, retrospective and flawed in various ways. Aiming for a MAP of > 85 for 5-7 days is recommended by guidelines but why this pressure and duration are good questions. Hypertensive therapy is relatively safe and easy to implement but not without risk. Tessa discusses the pros and cons, how this is managed practically and what the future may hold in this area.

Hypertensing Spinal Cord Injury - gold standard or wacky?

Hypertensing Spinal Cord Injury - gold standard or wacky?

Hypertensing Spinal Cord Injury - gold standard or wacky?

SMACC Conference

Mark Weedon takes us through the increasingly utilised concept of an optimal cerebral perfusion pressure (CPPopt) for each unique patient. He discusses the background to CPPopt, including intrcranial pressure (ICP), the Monroe Kelly hypothesis, neurovascular coupling, and cerebral autoregulation in health and following brain injury. He shows how intracranial pressure is affected by intracranial compliance and how this affects ICP waveforms. Cerebral perfusion pressure in relation to the Brain Trauma Foundation guidelines is covered including management of elevated ICP (EICP). The currently recommended tiered approach to managing cerebral perfusion pressure and EICP is mentioned citing recent guidelines. He uses a clinical case of a TBI to illustrate how the CPPopt can be ascertained and used to guide therapy, including the easy to perform “MAP Challenge”. Mark also describes the Pressure Reactivity Index (PRx) and how it can be used as a target for therapy. Finally, he covers the exciting results of the preliminary COGiTATE pilot study.

Optimal Cerebral Perfusion Pressure

Optimal Cerebral Perfusion Pressure

Optimal Cerebral Perfusion Pressure

SMACC Conference

The Power of Words - Death and Language.ppt

The Power of Words - Death and Language.ppt

The Power of Words - Death and Language.ppt

SMACC Conference

Appropriate use of antimicrobials is primarily a patient safety issue, and is the key aim of an effective antimicrobial stewardship program. We discuss the challenges in the management of a patient with sepsis, and how decision-making is usually done in the absence of effective diagnostics. Time dependent protocols and the knowledge that undertreatment of a patient with sepsis will lead to poor outcomes will lead to prescribing that may be driven by fear. Antimicrobial resistance is associated with over-use of antimicrobials but is usually not the immediate concern. Antimicrobial stewardship programs should work closely with sepsis teams to ensure that sepsis pathways are implemented across the whole hospital, and that key principles of judicious use are embedded within the clinical pathway.

Sepsis and Antimicrobial Stewardship - Two Sides of the Same Coin

Sepsis and Antimicrobial Stewardship - Two Sides of the Same Coin

Sepsis and Antimicrobial Stewardship - Two Sides of the Same Coin

SMACC Conference

Being able to prognosticate in the aftermath of a traumatic brain injury (TBI) is important as it assists with counselling patients and families. Moreover, it helps rationally allocate healthcare resources. However, due to the heterogenous nature of TBI and variable pre brain injury patient factors and post brain injury course, this has proven to be a difficult task. Large cohort studies have enabled improved accuracy in the prediction of 6 month mortality and unfavourable outcome. Furthermore, many of the factors that contribute to long-term outcome have also emerged. However, it is not yet possible to use them in prediction algorithms or mathematical models. There is emerging evidence that pre injury psychosocial and demographic factors may be of more relevance than injury severity. Moreover, that 'outcome' becomes increasingly subjective and complex as the post injury duration increases. We end with three brief vignettes which highlight the fraught nature of long term outcome prediction.

Brain injury outcomes and predictors

Brain injury outcomes and predictors

Brain injury outcomes and predictors

SMACC Conference

Plus de SMACC Conference (20)

Precision Medicine in Acute Brain Injury

Precision Medicine in Acute Brain Injury

Precision Medicine in Acute Brain Injury

CSD by Jeffcote Coda 22.pdf

CSD by Jeffcote Coda 22.pdf

CSD by Jeffcote Coda 22.pdf

Subdural Haemorrhage and MMA embolisation

Subdural Haemorrhage and MMA embolisation

Subdural Haemorrhage and MMA embolisation

Andy Neill - More neuroanatomy pearls for neurocritical care

Andy Neill - More neuroanatomy pearls for neurocritical care

Andy Neill - More neuroanatomy pearls for neurocritical care

The BONANZA Trial and PbTO2 Monitoring

The BONANZA Trial and PbTO2 Monitoring

The BONANZA Trial and PbTO2 Monitoring

Dilating the Dogma of Vasospasm

Dilating the Dogma of Vasospasm

Dilating the Dogma of Vasospasm

EVD Tips and Tricks

EVD Tips and Tricks

EVD Tips and Tricks

There is no such thing as mild, moderate and severe TBI - by Andrew Udy

There is no such thing as mild, moderate and severe TBI - by Andrew Udy

There is no such thing as mild, moderate and severe TBI - by Andrew Udy

TBI Debate - Mild, moderate and severe categories work

TBI Debate - Mild, moderate and severe categories work

TBI Debate - Mild, moderate and severe categories work

TBI: when to stop and when to give time

TBI: when to stop and when to give time

TBI: when to stop and when to give time

Ketamine in Brain Injury by Toby Jeffcote

Ketamine in Brain Injury by Toby Jeffcote

Ketamine in Brain Injury by Toby Jeffcote

Managing Complications of Chronic SCI by Bonne Lee

Managing Complications of Chronic SCI by Bonne Lee

Managing Complications of Chronic SCI by Bonne Lee

EEG and Status Eplilepticus by Tania Farrar

EEG and Status Eplilepticus by Tania Farrar

EEG and Status Eplilepticus by Tania Farrar

Browne Neuro symposium.pptx

Browne Neuro symposium.pptx

Browne Neuro symposium.pptx

Paediatric Stroke by Shree Basu

Paediatric Stroke by Shree Basu

Paediatric Stroke by Shree Basu

Hypertensing Spinal Cord Injury - gold standard or wacky?

Hypertensing Spinal Cord Injury - gold standard or wacky?

Hypertensing Spinal Cord Injury - gold standard or wacky?

Optimal Cerebral Perfusion Pressure

Optimal Cerebral Perfusion Pressure

Optimal Cerebral Perfusion Pressure

The Power of Words - Death and Language.ppt

The Power of Words - Death and Language.ppt

The Power of Words - Death and Language.ppt

Sepsis and Antimicrobial Stewardship - Two Sides of the Same Coin

Sepsis and Antimicrobial Stewardship - Two Sides of the Same Coin

Sepsis and Antimicrobial Stewardship - Two Sides of the Same Coin

Brain injury outcomes and predictors

Brain injury outcomes and predictors

Brain injury outcomes and predictors

Dernier

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